Stimulant Cardiotoxicity

[Xeromatosis]

What mechanism primarily effectuates the cardiotoxicity of psychostimulants?

Is it purely a consequence of long lasting overexertion? I know little about the heart but using most muscles seems to increase their efficiency and capacity.
What distinguishes the muscles in this case?

Or perhaps some chemicals are caustic to the heart and literally effect degeneration of the muscle and cell decay?
In this case does the cardiotoxicity of stimulants correlate with their active dose?

What information i've found also seems to indicate that psychostimulants induce cardiac hypertrophy,
but in this case shouldn't that enable more blood to enter the heart and consequently a lower beat rate and increased efficiency?
I'd cite athletic heart syndrome as example of this principle.

My only other conjecture was that drug generated vasoconstriction and resultant increases in blood pressure might cause the heart catastrophic stress?
Maybe even deformation?

I would have your wisdom and informed hypotheses.

 

[nAON]

I don't know a huge amount this, but I know one major cause of cardiotoxicity were drugs that affected 5HT-2C, which causes problems with heart valves.

Gonna move this to ADD, see if you can get a better response

BDD -> ADD

 

[sekio]

The main cardiotoxic stimulant I know of is cocaine, which is cardiotoxic by two actions - direct vasoconstriction of the heart tissue, and sodium channel block which impairs electrical conductivity.

The receptor that caused heartvalve overproliferation is 5-HT2B (not 2C). Fenfluramine ("Fen-Phen") got a whole lot of shit for increasing the rate of cardiac effects in regular users.

Normally, vasoconstrictive effects of stimulants used in safe doses and in moderation are not cardiotoxic per se.

 

[Xeromatosis]

sodium channel block which impairs electrical conductivity.

Hah, so of all its effects it's actually coke's anesthetic properties that are dangerous! Can't wait to try and convince the average user of that.
I never would have guessed that it would actually prevent action potentials from occurring, i'd assumed there must be more longterm, macroscopic damage. Literally a heart-stopper then huh.
So i guess snorting something apparently harmless like benzocaine could just as soon freeze my thumper?

The receptor that caused heartvalve overproliferation is 5-HT2B

-_- i would have suspected an adrenergic receptor the culprit. Time to cut back on that DMT i suppose.

 

[sekio]

I think it's chronic overstimulation that's the problem. Psychedelics actually haven't been shown to cause heart damage.

Just stay away from the daily MDA/MDMA/fenfluramine, and you'll be good...

Of course monoaminergic stimulants are mostly all vasoconstrictors as well, this leads to increased blood pressure and all the resulting risks associated with it like stroke and cardiac damage. Phenylpropanolamine (N-desmethylephedrine) was recalled from most markets because it increased the risk of stroke appreciably.

 

[alkap555]

Cocaine cardiotoxicity: a review of the pathophysiology, pathology, and treatment options

Numerous mechanisms have been postulated to explain how cocaine contributes to these conditions. Among these, cocaine may lead to MI by causing coronary artery vasoconstriction and accelerated atherosclerosis, and by initiating thrombus formation. Cocaine has also been shown to block K+ channels, increase L-type Ca2+ channel current, and inhibit Na+ influx during depolarization, all possible causes for arrhythmia. Additionally, cocaine use has been associated with left ventricular hypertrophy, myocarditis, and dilated cardiomyopathy, which can lead to heart failure if drug use is continued.

http://www.ncbi.nlm.nih.gov/pubmed/19463023